Saudi Journal of Kidney Diseases and Transplantation

: 2010  |  Volume : 21  |  Issue : 6  |  Page : 1115--1117

Infection with Histoplasma capsulatum in a renal transplant recipient

Arcot Rekha1, Anupma Jyoti Kindo2, P Sounderarajan3, A Ravi1,  
1 Department of Surgery, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai, India
2 Department of Microbiology, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai, India
3 Department of Nephrology, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai, India

Correspondence Address:
Arcot Rekha
Department of Surgery, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai


With the advent of potent immunosuppressive therapies in solid organ trans­plantation, patients are more susceptible to a variety of infections with atypical pathogens and presentations. We report a renal transplant recipient with atypical presentation of histoplasmosis.

How to cite this article:
Rekha A, Kindo AJ, Sounderarajan P, Ravi A. Infection with Histoplasma capsulatum in a renal transplant recipient.Saudi J Kidney Dis Transpl 2010;21:1115-1117

How to cite this URL:
Rekha A, Kindo AJ, Sounderarajan P, Ravi A. Infection with Histoplasma capsulatum in a renal transplant recipient. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2021 Oct 18 ];21:1115-1117
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Full Text


Histoplasmosis is a fungal infection caused by the dimorphic saprophytic fungus Histoplasma capsulatum, which is endemic in the Central United States, South America, the Caribbean, Africa, and Asia. However, microfoci are be­lieved to occur anywhere with warm humid soil. [1] In patients on immunosuppression, prog­ressive disseminated disease has a high morta­lity rate of 7-23%. [2] Clinical manifestations vary (depending on host's immunity and size of inoculum) from a mild transient flu-like illness to rapidly progressive, often fatal, disseminated disease. [1] An awareness of this uncommon pa­thogen is necessary for the clinician to diag­nose this disease, utilize the investigative mo­dalities and initiate appropriate treatment.

 Case Report

A 47- year- old man from Burma came to our hospital in South India with a complaint of fe­ver for 1 month. He had type 2 diabetes mellitus (11 years duration) and undergone renal trans­plant 3 years prior to his current complaint and had been on immunosuppressant therapy with cyclosporine, azathioprine and steroids.

Physical examination disclosed normal blood pressure, but detected a swelling (3 × 4 cms) in the medial aspect of his right arm 5 cm proxi­mal to the cubital fossa and also another swelling (5 × 6 cms) over the dorsum of the right wrist joint [Figure 1]. It was not warm or tender and consistency was variable (soft, fluctuant in some areas, firm in others).There were no palpable lymph nodes and there was no fixation to un­derlying muscles, bone or overlying skin.{Figure 1}

The laboratory investigations revealed hemo­globin (HB) 11.7 g/dL, leukocyte count 9800/ mm 3 , urea 75 mg/dL, creatinine 1.8 mg/dL, cal­cium 8.5 mg/dL, phosphate 3.7 mg/dL, alkaline phosphatase 70 IU, bilirubin 0.7 mg/dL, normal liver enzymes (SGOT 33 IU and SGPT 26 IU), and normal sugar levels. Computerized tomo­graphy (CT) scan of the chest was normal cytomegalovirus titers were negative.

A fine needle aspiration count (FNAC) of the swelling was inconclusive and an excision biopsy of the right arm swelling was done. Gomori's Methanamine silver stain (GMS) of the biopsy specimen showed plenty of oval, narrow based budding intracellular yeast cells suggestive of Histoplasma capsulatum [Figure 2]. The diagnosis was confirmed by culture in Sabouraud's dextrose agar and brain heart in­fusion agar. The tubes showed a white compact growth after 3 weeks of incubation at 25ºC. Lactophenol cotton blue mount showed narrow septate hyphae with typical spikes on the wall of the conidia [Figure 3]. Urease test differen­tiated between H. capsulatum and H. dubiosii, and dimorphism was demonstrated by conver­ting the H. capsulatum into yeast forms at 37ºC in brain heart infusion agar.{Figure 2}

The patient was started on amphotericin B 50 mg i.v. for 24 days and T. itraconazole 100 mg orally. Four weeks later, there was no residual lesion left on the upper limb.


The vast majority of primary infection with Histoplasma capsulatum (> 90%) causes sub­clinical disease. Central nervous system in­volvement is rare and is seen in transplant patients. When chest infection is present, chest radiographic findings include diffuse, nodular, patchy, or military infiltrates; hilar adenopathy is uncommon. [3],[4] The elderly, those younger than 2 years of age, and individuals whose im­mune system are compromised are more likely to develop a progressive and disseminated di­sease.

Primary infection is acquired by inhalation of infectious microconidia, by direct inoculation into skin, or via an infected allograft. [5] Once the microconidia is lodged in the alveolar and interstitial spaces, it becomes a yeast, multi­plies intracellularly and disseminates until cell mediated immunity develops (2-10 weeks). [6]

Disseminated disease is marked by fever, weight loss, weakness, fatigue and mild respiratory symptoms. The most common symp­tom of infection is fever, and often associated with cutaneous and subcutaneous lesions as shown in [Figure 3].{Figure 3}

Cutaneous lesions in disseminated histoplas­mosis include papules, nodules, plaques, ery­thema multiforme-like lesions, and exfoliative dermatitis. [7] Erythema nodosum, a hypersensi­tivity mediated panniculitis in which the orga­nisms are not present has also been described. [8] Gomori's methanamine silver stain is the best stain for H. capsulatum. The organisms are seen as numerous, small (2-4 μm), oval yeast like fungi within the cytoplasm of macrophages in the dermis and subcutaneous tissue.

Definite diagnosis is made by a combination of culture of the organism, detection of it in tissues, measurement of antibodies, or antigen detection. [3] Disseminated histoplasmosis is a life threatening illness if not diagnosed and appro­priately treated.

Amphotericin B is the drug of choice for in­duction therapy. Liposomal amphotericin does not have renal toxicity. However, as it is very costly, we administered conventional ampho­tericin B to our patient without any problems. The recommended dose of conventional am­photericin B is 0.7-1 mg/day with a cumulative dose of approximately 35 mg/kg. [9] This treat­ment must be followed with itraconazole (200 mg/day for 1 year or more) maintenance the­rapy to reduce relapse rate.

In conclusion, cutaneous lesions may be the only sign of serious systemic disease in post transplant immunosuppressed patients, as seen in our case. Transplant physicians need to be aware of this presentation, as appropriate timely investigations and optimal treatment are asso­ciated with good outcome.


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